Management of Varicose

Veins and Lymphedema

Venous Anatomy

 The venous system in the lower limbs is

made up of a number of complex
anatomical structures, including
principally:
1. The deep venous system
2. The superficial venous system
3. Perforating veins

Deep Venous System

The deep venous system, located in the
central axis of the leg, follows the arteries
and is surrounded by muscles and
aponeurosis. (The veins have the same
names as the arteries that they run
alongside: iliac, femoral, popliteal, fibular,
tibial veins)

Superficial Venous System

The superficial venous system varies greatly from one
person to another. This network of veins is located
primarily in the subcutaneous adipose layer, between
the wall of the skin and the aponeurosis encasing the
muscles. The main two components of the superficial
venous system are :
The great saphenous (or greater saphenous) vein, which
runs up the inner surface of the calf and thigh before joining
the femoral vein,
The small saphenous (or lesser saphenous) vein, located on
the posterior surface of the calf and draining into the
popliteal vein.

Perforating Veins
Cross the aponeurosis to link deep
and superficial veins

Physiology of Venous System

The main purpose of the venous system within
the general circulation, is to carry oxygendepleted blood rich in cell metabolism waste
back to the heart.
It is within the legs that the stresses are the
greatest and the specific characteristics of the
venous system are the most important,
since the venous system must move blood
against the force of gravity in the standing
position .

 A combination of two main actions ensures

venous return in the lower limbs:
Firstly, the presence of mobile anti-reflux
valves and the resistance of the vein walls
allowing the blood to move in one direction
only : from the superficial to towards the deep
venous system and from the feet to the heart.
Secondly, a pump mechanism which activates
and maintains the blood flow through the veins.

 The anti-reflux valves allow fluid to circulate in

one direction only, making it possible to
maintain the normal direction of venous blood
flow, even in the absence of pressure or in
the event of negative pressure and thereby
prevent backflow of the blood.
Normal blood flow is directed from the
superficial towards the deep system and from
the most distal part of the body towards the
heart.

The pump mechanism mainly results

from a combination of different forces:
The stimulation of the venous system of the foot
The muscle pump, more specifically, the
muscles of the calf (leading to alternate opening
and closing of the valves): which is the main
driving force behind the pump mechanism,
The beating of the heart and the negative
pressure due to the phenomenon of aspiration
from the abdominal cavity that occurs during
deep breathing.

Pathophysiology of Chronic
Venous Diseases

1. Valve Insufficiency
This may be quantitative or qualitative
Quantitave in the event of congenital
insufficiency in terms of valve numbers or
massive destruction due to venous
thrombosis
Qualitative as a result of a valve being torn or
due to permeability of the valve

2. Venous Wall Damage

Damage to the venous wall seems to be more common than valve damage. The wall
becomes thinner at the level of the valve. The vein is dilated and pushes the valve
cusps apart, compromising their impermeability. This wall damage may be related to
damage to the innermost layer of the vein: the endothelium.
Hereditary factors, sedentary lifestyle, age,
Deficiency of the muscle and joint pump
Female sex hormones, enzymatic factors,
Sequestration of leukocytes and their adhesion to the endothelium
Microcirculatory problems
Defective vasoconstriction in the standing position
Hypercoagulability of blood in the event of a thrombosis

Damage to valves and the venous wall under the influence of one or more of the above
factors will lead to impairment of the venous network of the lower limbs. It causes venous
hypertension which can lead to a chronic venous disease with tissue decompensation:
chronic venous insufficiency.

3. Venous Hypertension
In the supine position, the venous pressure at the ankle is ~ 15mmHg and
in the sitting position, ~ 55mmHg.
In the standing position, the venous pressure at the ankle, which is around
90 mmHg in a healthy individual, can exceed 100 mmHg in an individual
suffering from severe CVI (chronic venous insufficiency).
When walking, the dynamic anatomical structures which control venous
return are activated and the venous pressure at the ankle falls gradually
with each step until it levels out at around 20-25 mmHg for a healthy
individual.
In the event of CVD, the venous pressure at the ankle does not fall to such
low values due to stagnation of fluid, inducing venous hypertension. In the
event of severe CVD, pressure on walking can be significantly higher than
normal, reaching a value of 70 mmHg, reflecting marked venous
hypertension.

4. Visible Morphological Changes

As a result of this excessive pressure and
defective peripheral vasoconstriction, the
venous wall gradually stretches. Varicose
veins appear.

5. Tissue Changes
Haemodynamically, CVD is manifested by stagnation or stasis of
fluids leading to an increase in venous pressure (more marked
distally than proximally), combined with a reduction in venous wall
resistance and dilation of the vein diameter. All this leads to the
valve cusps being moved further apart, causing them to become
incompetent.
The increase in venous pressure is passed on to the capillaries,
causing tissue oedema and extravasation of blood elements, which
participate in the release of inflammation mediators.
Oedema, initially reversible, gradually sets in and becomes chronic.
Over the years, it becomes more specific, becoming enriched with
proteins and forming interstitial fibrosis.

 In addition, interstitial flooding creates conditions

favourable to the formation of local tissue
ischaemia and trophic problems: atrophie
blanche, varicose eczema, pigmented purpuric
dermatitis, etc.

Varicose Veins
Long, tortuous and dilated vein
of the superficial varicose system

Pathophysiology
One-way venous valves are found in both systems and the
perforating veins.
Incompetence in the superficial venous system alone
usually results from failure at valves located at the SFJ and
SPJ.
Incompetence of the perforating veins leads to
hydrodynamic pressure. The pressure generated in the
deep venous system by the calf pump mechanism are
transmitted into the superficial system via the incompetent
perforating veins
Pooled blood and venous hypertension leads to venous
dilatation, which then causes greater valvular insufficiency.

Signs and Symptoms

Aching, heavy legs (often worse at night and after exercise).

Appearance of spider veins (telangiectasia) in the affected leg.
Ankle swelling, especially in evening.
A brownish-yellow shiny skin discoloration near the affected
veins.
Redness, dryness, and itchiness of areas of skin, termed
stasis dermatitis or venous eczema, because of waste
products building up in the leg.
Cramps may develop especially when making a sudden move
as standing up.
Minor injuries to the area may bleed more than normal or take
a long time to heal.

History
History of venous insufficiency (eg, date of onset of visible abnormal vessels, date of
onset of any symptoms, any known prior venous diagnoses, any history of pregnancyrelated varices)
Presence or absence of predisposing factors (eg, heredity, trauma to the legs,
occupational prolonged standing, sports participation)
History of edema (eg, date of onset, predisposing factors, site, intensity, hardness,
modification after a night's rest)
History of any prior evaluation of or treatment for venous disease (eg, medications,
injections, surgery, compression)
History of superficial or deep thrombophlebitis (eg, date of onset, site, predisposing
factors, sequelae)
History of any other vascular disease (eg, peripheral arterial disease, coronary artery
disease, lymphedema, lymphangitis)
Family history of vascular disease of any type

Physical Examination

Surgical scars from prior intervention

Pigmentations and skin changes (lipodermatosclerosis)
Varicose veins
Ulcers of the medial ankle

 Palpate the saphenofemoral junction (SFJ). It is best

palpated 2 fingerbreadths below the inguinal ligament
and just medial to the femoral artery. If reflux is present,
a forced coughing maneuver may produce a palpable
thrill or sudden expansion at this level.
The posterior surface of the calf is the territory of the
short saphenous vein. This may be palpable in the
popliteal fossa in some slender patients.
Palpation of an area of leg pain or tenderness may
reveal a firm, thickened, thrombosed vein.
With the patient in a standing position, a vein segment is
percussed at one position while an examining hand feels
for a "pulse wave" at another position.

Special Test
Trendeleburg Test
This can sometimes distinguish patients with superficial venous
reflux from those with incompetent deep venous valves.
The patient should lie flat with the leg elevated, allowing the veins
to empty. A tourniquet is applied to the thigh at the saphenous
opening. If the valve is competent, the vein should fill from below.
If the valve is incompetent, the vein will fill from above on removal
of the tourniquet.
The test can be repeated with the tourniquet at different levels to
further pinpoint the level of valvular incompetence:
above the knee - to assess the mid-thigh perforators
below the knee - to assess incompetence between the short
saphenous vein and the popliteal vein.

 Perthes Test
This manoeuvre is used to distinguish antegrade flow
from retrograde flow in superficial varicosities.
A tourniquet is applied to a varicose leg in such a way
that the superficial veins are compressed without
pressure being applied to the deep vessels. The patient
is then asked to stand repeatedly on tiptoe, activating the
calf muscles. Normally this would empty the varicosities
but, in the presence of deep vein obstruction, they would
paradoxically become congested.